ABSTRACT
Adhesion is the primary functional manifestation of platelets. These cellular elements of the hemostatic system are the first to become activated when this complex system of cells, clotting factors, and their inhibitors are called upon to stem the flow of blood from a vessel that has lost its continuity. The interaction of platelets with specific elements of the vessel wall represents the first event that in time leads to formation of a firm clot composed of a fibrin meshwork intimately linked to platelets and intermingled to varying degrees with red cells. Platelets normally circulate in blood as small, oblate ellipsoids that shun interaction with each other and are shielded from adhesive surfaces by the continuum of the endothelial surface lining the blood vessels. Contact with certain agonists, however, induces a profound morphological and ultrastructural reorganization, which also renders the surface of the platelet sticky and ready to interact with adhesive proteins. This altered reactivity of platelet membranes, as well as their change in shape from a discoid structure to a spiny sphere, can also be induced by shear forces of varying strength. The latter represents an exceedingly important mechanism of platelet activation, especially under pathological circumstances where flow alterations due to inhomogeneities in the wall may be a prominent feature.
